Changes in the responsiveness of parabrachial neurons in the arthritic rat: an electrophysiological study.

1. Rats rendered polyarthritic by injection of Mycobacterium butyricum into the tail were used as a model for the study of "chronic pain". In such rats, anesthetized with halothane in a nitrous oxide-oxygen mixture, spontaneous activity and responses of parabrachial (PB) neurons to somatic stimulations were studied in comparison with those in a control group of healthy animals processed under the same experimental conditions. 2. The size of the somatic receptive field of PB neurons was similar in both arthritic and control groups. In the control group 13%, 55%, and 32% of the receptive fields were small, medium, and large, respectively. Similarly, in the arthritic group, 10%, 60%, and 30% of the receptive fields were small, medium, and large, respectively. 3. The spontaneous activity was significantly (P < 0.001) increased in the arthritic rats (0.1 < 3 < 16 Hz, n = 31; 10th percentile < median < 90th percentile) in comparison with the healthy rats (0.03 < 0.3 < 5 Hz, n = 22). 4. The sensitivity to mechanical stimuli was markedly increased in arthritic compared with healthy rats: 1) although PB neurons in normal rats never responded to innocuous stimuli, several PB neurons in arthritic rats responded to touch and/or joint movement; 2) the mean mechanical threshold decreased from 15.8 N/cm2 in normal rats to 5.9 N/cm2 in arthritic rats; 3) the mean pressure evoking 50% of the maximum response decreased from 34 N/cm2 in normal rats to 21 N/cm2 in arthritic rats; and 4) the intensity of the maximum response increased from 15.7 Hz in normal rats to 26.3 Hz in arthritic rats. 5. The mechanical encoding properties were clearly modified in arthritic rats compared with healthy rats. In this latter group, the PB neurons exhibited a clear capacity to encode mechanical stimuli in the noxious range: 1) the stimulus-response curves were always positive and monotonic until 48 N/cm2; and 2) the slope of the mean curve increased progressively from 2 to 8 N/cm2 before reaching a roughly linear maximum for a wide range of pressure (8-64 N/cm2) and plateauing beyond. In the arthritic rat, the PB neurons also encoded mechanical stimuli, but clearly from a lower pressure range: the slope of the mean curve was maximum and remained steep from the lowest pressure tested (1 N/cm2) up to 16 N/cm2; afterward the slope decreased progressively from 16 to 64 N/cm2 before plateauing. 6. The sensitivity to heat stimuli was only weakly modified. The thermal threshold was weakly, but significantly, increased from 44 degrees C in the normal rat to 45.8 degrees C in the arthritic rat. Other parameters for thermal modality were not changed, with the mean stimulus-response curves being similar in both arthritic and normal groups. 7. In conclusion, these experiments demonstrate that the activity of PB neurons is clearly changed in arthritic rats. These changes are reminiscent of some behavioral and electrophysiological modifications observed during arthritis. Considering the current literature, it is hypothesized that the PB relay could be responsible, at least in part, for several affective-emotional, behavioral, autonomic, and energy metabolism changes observed in arthritic rats.